LOWER GI PATHOLOGY

Inflammatory conditions

active

neutrophil infiltration (characteristic), cryptitis, normal architecture

chronic

crypt architectural distortion (branching/shortening)

active chronic inflammation - acute + evidence of chronicity

crypt abscesses (neutrophil infiltration into lumen of crypts)

Infective colitis

Ischaemic colitis

Diverticulitis

Idiopathic IBD

acute colitis

acute colitis

active or active chronic colitis

active chronic colitis

pseudomembranous colitis

due to C. difficile infection following broad spectrum antibiotics

neutrophils form 'membrane' on top of mucosa

acute inflammation, neutrophils, mild crypt loss

watery diarrhoea, colicky abdominal pain, fever

usually superficial

if penetrates through the colon wall, causes infarction

mixed acute and chronic inflammation, crypt loss

lack of O2 supply (usually due to decreased blood flow)

causes: arterial/venous occlusion, vasculitis, intestinal obstruction

most commonly occurs in the watershed area around splenic flexure/descending colon

between supply of middle and left colic arteries

outpouching of mucosal wall (where muscle is weakest)

bacteria can overgrow here

if obstructed, they perforate or form diverticular abscess

bleeding, perforation, abscess, fistula (if adherent to other structures), stricture

Ulcerative colitis

acute

marked hyperaemia and irregular ulceration

chronic

diffuse ulceration with focal residual mucosa

pseudopolyps (formed by regenerating mucosa)

total mucosal atrophy and crypt flattening (late)

diffuse active inflammation confined to mucosa

basal plasmacytosis, crypt distortion

complications

toxic megacolon (perforation)

dysplasia and carcinoma (>20 years)

Crohn's disease

involves any site in GIT (most commonly terminal ileum)

patchy (skip lesions)

affects full thickness of bowel wall

fat wrapping

thick rigid wall

longitudinal ulceration with sharp demarcation

cobblestone appearance (due to regenerating mucosa between ulcerations)

deep fissures

muscle and neural hypertrophy

granulomas in 50%

collection of epithelioid histiocytes (macrophages)

complications

adhesions, perforations, abscess, fistula, stricture, dysplasia/carcinoma

Neoplastic disease

primary

secondary

metastasis

epithelial (most common)

Lymphoid

soft tissue

glandular epithelium

adenoma (polyp)

carcinoma

neuroendocrine cells

neuroendocrine tumour

sessile (flat on surface)

pedunculated (long stalk of mucosa)

neoplastic

non-neoplastic

adenomatous polyp

serrated polyp

reactive (inflammatory or traumatic)

hyperplastic

hamartomatous (developmental)

Peutz-Jegher's polyp

juvenile polyp

tubular adenoma

villous adenoma

tubulovillous adenoma

typically sessile

typically pedunculated

traditional serrated

sessile serrated

most polyps are sporadic not genetic

familial polyposis syndromes

familial adenomatous polyposis (FAP)

100+ polyps

develop carcinoma <40 years (100%)

total colectomy

abnormal glandular tissue

chromosome instability pathway

oncogenes (e.g. ß-catenin) and tumour suppressor genes (e.g. APC, e-cadherin)

tend to be left-sided carcinomas

microsatellite instability pathway

DNA mismatch repair due to gene mutation or promoter methylation (silencing)

tend to be right-sided carcinomas

better prognosis

autosomal dominant mutation of APC gene (Ch5)

attenuated FAP

MYH or APC gene (other loci)

less than 100 polyps

lynch (HNPCC)

less than 100 polyps

DNA mismatch repair genes MSH2/MLH1/MSH6/PMS2

risk of developing carcinoma >50 years

risk of developing carcinoma 45-50 years